The etiology for chronic abdominal

The etiology for chronic abdominal bloating and distension is complex, oftenmultifactorial in nature, and incompletely understood. The differential diagnosis includes bothorganic and functional disorders (see Table 2). Most patients believe that their symptoms aredue to an increased amount of “gas” within the gastrointestinal (GI) tract, although this accountsfor symptoms in only a minority of patients. Normal gas production, absorption, and excretionare illustrated in Figure 1. CT imaging has shown that luminal gas increases in only 25% ofpatients with FGIDs during a spontaneous episode of abdominal distension or followingconsumption of a “high-flatulence” diet (14). The following sections highlight majorpathophysiologic causes of bloating and distension (see Figure 2).Small intestinal bacterial overgrowth and carbohydrate intoleranceSmall intestinal bacterial overgrowth (SIBO) and carbohydrate (e.g., lactose and fructose)intolerance are common causes of chronic bloating and distension. Excess small intestinebacteria can cause symptoms due to carbohydrate fermentation with subsequent gas productionand stretch and distension of the small intestine. Altered sensation and an abnormalviscerosomatic reflex may also play a role although these mechanisms have not been wellstudied in patients with SIBO. Carbohydrate intolerance may cause symptoms of bloating and 5distension due to an increased osmotic load, excess fluid retention, and excess fermentation inthe colon. The lack of consensus regarding an ideal test to diagnose SIBO makes it difficult toascertain its true prevalence. In addition, no prospective trial has evaluated patients diagnosedsolely with chronic bloating and distension to determine the prevalence of SIBO or foodintolerances, and thus most data comes from the best studied functional gastrointestinal disorder,IBS. A meta-analysis reported the prevalence of SIBO to be 0-20% in healthy controls versus 4-78% in patients with IBS (15). The prevalence of food intolerance, which has similar symptoms,in the general population approaches 20% (16). The true prevalence of carbohydrate intoleranceis unclear as carbohydrate intolerance does not necessarily correspond with carbohydratemalabsorption by breath test. One prospective study of symptomatic patients with variousFGIDs (n = 1372) identified a prevalence of lactose intolerance and malabsorption of 51% and32% respectively, and a prevalence of fructose intolerance and malabsorption of 60% and 45%respectively (17). Lactase deficiency by itself may not cause malabsorption, as not allindividuals who are lactase deficient become symptomatic after ingesting lactose. This indicatesthat other factors (e.g., genetic predisposition, visceral hypersensitivity) may be required forsymptom generation in some patients.